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Arterial gas embolism is a potentially catastrophic event that occurs when gas bubbles enter or form in the arterial vasculature and occlude blood flow, causing organ ischemia. Arterial gas embolism can cause CNS ischemia with rapid loss of consciousness, other CNS manifestations, or both; it also may affect other organs. Diagnosis is clinical and may be corroborated by imaging tests. Treatment is immediate recompression.

Gas emboli may enter the arterial circulation in any of the following ways:

• From ruptured alveoli after lung barotrauma
• From within the arterial circulation itself in severe decompression sickness
• Via migration from the venous circulation (venous gas embolism) either via a right-to-left shunt (patent foramen ovale, atrial septal defect) or by overwhelming the filtering capacity of the lungs

Even asymptomatic venous gas embolism can cause serious manifestations (eg, stroke) in the presence of a right-to-left shunt. Venous gas embolism that does not enter the arterial circulation is less serious.

Although cerebral embolism is considered the most serious manifestation, arterial gas embolism can cause significant ischemia in other organs (eg, spinal cord, heart, skin, kidneys, spleen, GI tract).

Symptoms and Signs

Symptoms occur within a few minutes of surfacing and may include altered mental status, hemiparesis, focal motor or sensory deficits, seizures, loss of consciousness, apnea, and shock; death may follow. Signs of pulmonary barotrauma (see Drowning: Symptoms and Signs) or type II decompression sickness (see Injury During Diving or Work in Compressed Air: Symptoms and Signs) may also be present.

Other symptoms may result from arterial gas embolism in any of the following:

• Coronary arteries (eg, arrhythmias, MI, cardiac arrest)
• Skin (eg, cyanotic marbling of the skin, focal pallor of the tongue)
• Kidneys (eg, hematuria, proteinuria, renal failure)

Diagnosis

• Clinical evaluation
• Sometimes confirmation by imaging

Diagnosis is primarily clinical. A high level of suspicion is necessary when divers lose consciousness during or immediately after ascent. Confirming the diagnosis is difficult because air may be reabsorbed from the affected artery before testing. However, imaging techniques that may support the diagnosis (each with limited sensitivity) include the following:

• Echocardiography (showing air in the cardiac chambers)
• Ventilation-perfusion scan (showing results consistent with pulmonary emboli)
• Chest CT (showing local lung injury or hemorrhage)
• Head CT (showing intravascular gas and diffuse edema)

Sometimes decompression sickness can produce similar signs and symptoms (for a comparison of features, see Table 1: Injury During Diving or Work in Compressed Air: Comparison of Gas Embolism and Decompression Sickness).

Table 1
Comparison of Gas Embolism and Decompression Sickness Feature Gas Embolism Decompression Sickness Symptoms and signs Common: Unconsciousness, often with seizures (any unconscious diver should be assumed to have gas embolism and should be recompressed promptly) Less common: Milder cerebral manifestations, signs of pulmonary barotrauma, such as mediastinal or subcutaneous emphysema and pneumothorax Extremely variable—the bends (pain, most often in or near a joint), neurologic manifestations of almost any type or degree, and the chokes (respiratory distress followed by circulatory collapse—an extreme emergency), occurring alone or with other symptoms Onset Sudden, usually during or within a few minutes after surfacing Gradual or sudden, with symptoms developing ≥ 1 h after surfacing in about 50%, onset up to 24 h after dives* of > 10 m (> 33 ft) or hyperbaric exposures of > 2 atm abs Proximate cause Usual: Breath holding or airway obstruction during ascent, even from a few feet of depth particularly when ascent is rapid, or decompression from increased pressure Usual: Diving or hyperbaric exposure beyond no-stop limits and without appropriate decompression stops Occasional: Diving or hyperbaric exposure within no-stop limits or with appropriate decompression stops; low-pressure exposure (eg, flying after diving) Mechanism Usual: Overinflation of lungs causing entry of free gas into pulmonary vessels followed by embolization of cerebral vessels Occasional: Coronary, renal, or cutaneous circulatory obstruction by free gas from any source Formation of bubbles from excess dissolved gas in blood or tissue when external pressure decreases Emergency treatment Essential emergency care as needed (eg, airway patency, hemostasis, cardiopulmonary resuscitation or mechanical ventilation) Prompt transport to nearest recompression chamber Horizontal position 100% O2 by close-fitting mask Fluids orally if patient is conscious; otherwise, IV Essential emergency care as needed (eg, airway patency, cardiopulmonary resuscitation or mechanical ventilation) Prompt transport to nearest recompression chamber 100% O2 by close-fitting mask Fluids orally if patient is conscious; otherwise, IV atm abs = atmospheres absolute. *Repeat dives are frequently involved.

Treatment

• Immediate 100% O₂
• Recompression therapy

Divers thought to have gas embolism should be recompressed promptly (see Injury During Diving or Work in Compressed Air: Recompression Therapy). Transport to a recompression chamber takes precedence over nonessential procedures. Transport by air may be justified if it saves significant time, but exposure to reduced pressure at altitude must be minimized (see Injury During Diving or Work in Compressed Air: Treatment).

Before transport, high-flow 100% O₂ enhances N₂ washout by widening the N₂ pressure gradient between the lungs and the circulation, thus accelerating reabsorption of embolic bubbles. Patients should remain in a supine position to decrease the risk of brain embolism. Mechanical ventilation, vasopressors, and volume resuscitation are used as needed. Placing patients in the left lateral decubitus position (Durant's maneuver) or Trendelenburg position is no longer recommended.

Last full review/revision April 2009 by Alfred A. Bove, MD, PhD

Content last modified April 2009